Misdiagnosed Cerebral Venous Sinus Thrombosis in the Puerperium A Multidisciplinary Case Review
- OBGYN Library Team
- Aug 26
- 8 min read
A severe headache in the first weeks after delivery is common enough to be dismissed, yet dangerous enough to demand respect. In the puerperium, headache may reflect sleep deprivation, migraine, post-dural puncture headache, eclampsia, meningitis, subarachnoid haemorrhage, or cerebral venous sinus thrombosis. The overlap is exactly why delayed diagnosis occurs.
CEREBRAL VENOUS SINUS THROMBOSIS is uncommon, but the puerperal period is a recognised high-risk window. Physiological hypercoagulability, dehydration, infection, caesarean delivery, anaemia, thrombophilia, and reduced mobility can all contribute. The condition is treatable, and outcomes can be good when teams recognise it early and start anticoagulation promptly.
This article presents an anonymised composite case for educational use, followed by a literature-based review of diagnosis and multidisciplinary management. It is informational only and does not replace local protocols or specialist judgement.
Case report of a delayed diagnosis in the first postpartum week
A 28-year-old woman, gravida 2 para 2, delivered a healthy infant by emergency lower-segment caesarean section for foetal distress. She had no known thrombophilia, no history of seizures, and no prior migraine. Her antenatal course was mostly uncomplicated apart from mild iron-deficiency anaemia. She received spinal anaesthesia, routine perioperative antibiotics, and standard postoperative care.
On postpartum day 4, she developed a dull, diffuse headache. It was worse on sitting and improved slightly on lying down. She also reported nausea and photophobia. Her blood pressure was 128/82 mmHg, she was afebrile, and there was no neck stiffness. The initial impression was post-dural puncture headache or migraine. She was advised hydration, caffeine-containing fluids, paracetamol, and observation.
By postpartum day 6, the headache became severe and persistent. It no longer had a clear postural component. She vomited twice and described blurred vision. A repeat blood pressure reading showed 142/90 mmHg. Urine dipstick showed trace protein. Given the timing, eclampsia spectrum disease was considered. She received magnesium sulphate prophylaxis while blood tests were sent.
Platelet count, liver enzymes, serum creatinine, and coagulation profile were within acceptable ranges. Haemoglobin remained low at 9.2 g/dL. There was no fever or leucocytosis to suggest sepsis. Fundus examination could not be completed because she was photophobic and restless. The headache was still attributed to a mixed picture of post-spinal headache and possible postpartum hypertension.
That evening, she had a focal seizure involving the right upper limb, followed by secondary generalisation. After recovery, she remained drowsy and had mild expressive difficulty. There was subtle right-sided pronator drift. These new focal findings changed the diagnostic pathway.
A non-contrast CT brain showed a left parietal haemorrhagic venous infarct with surrounding oedema. There was no aneurysmal pattern of subarachnoid haemorrhage. MRI brain with MR venography was performed next. It showed thrombosis of the superior sagittal sinus extending into the left transverse sinus, with cortical vein involvement.
The diagnosis was cerebral venous sinus thrombosis in the puerperium, initially mislabelled as post-dural puncture headache, migraine, and possible eclampsia.
Why the diagnosis was missed
The diagnostic delay in this case was not due to negligence or a single missed fact. It reflected a common problem in postpartum medicine: several serious conditions share the same early symptoms.
The headache sounded familiar at first
A postural headache after spinal anaesthesia makes clinicians think of post-dural puncture headache. That diagnosis was plausible on day 4, especially with nausea and photophobia. Yet the later evolution was not typical. The pain became progressive, lost its postural nature, and developed neurological associations.
A changing headache pattern in the puerperium should trigger reassessment. The first label may be wrong, or a second pathology may have emerged.
Blood pressure created diagnostic anchoring
Postpartum hypertension and eclampsia remain critical diagnoses. Magnesium sulphate was reasonable when blood pressure rose and headache persisted. Still, a near-normal preeclampsia laboratory profile and the presence of focal neurological signs should push clinicians towards neuroimaging.
Eclampsia can occur without dramatic hypertension, but focal deficits, aphasia, lateralising seizures, papilloedema, or reduced consciousness need imaging, even if magnesium is already being given.
Early CT may be normal
Non-contrast CT is fast and useful for haemorrhage, mass effect, and some infarcts, but it may not detect early venous sinus thrombosis. MRI with MR venography, or CT venography when MRI is unavailable, provides more direct evidence of sinus occlusion. In many hospitals, the need to escalate from CT to venography is the key diagnostic step.
Treatment and multidisciplinary management
Once the diagnosis was established, the patient was shifted to a high-dependency unit. Management involved obstetrics, neurology, radiology, haematology, anaesthesia, critical care, nursing, physiotherapy, and lactation support.
Acute stabilisation
During the seizure, airway protection, lateral positioning, oxygenation, and intravenous access were prioritised. She received an antiepileptic drug, levetiracetam, after neurology review. Magnesium sulphate was discontinued once eclampsia became less likely and the seizure was attributed to venous infarction, though this decision must be individualised.
Head elevation, fluid balance, pain control, and close neurological observations were started. The team avoided dehydration because haemoconcentration may worsen thrombosis. At the same time, fluids were not given blindly because cerebral oedema was present.
Anticoagulation despite haemorrhagic infarction
A frequent source of hesitation is the presence of intracerebral haemorrhage. In venous infarction, haemorrhagic transformation does not automatically contraindicate anticoagulation. Current guidance generally supports therapeutic anticoagulation with low-molecular-weight heparin or unfractionated heparin in acute CVST, unless there is a specific contraindication.
In this case, therapeutic low-molecular-weight heparin was started after discussion between neurology, obstetrics, haematology, and radiology. Platelet count, renal function, wound status, and bleeding risk were reviewed. The caesarean wound was monitored closely. No wound haematoma developed.
Unfractionated heparin may be preferred when rapid reversal is needed, renal function is poor, or neurosurgical intervention is anticipated. Low-molecular-weight heparin is often practical when renal function is normal and the patient is clinically stable.
Managing raised intracranial pressure and complications
The patient had papilloedema on formal ophthalmology examination. There was no large mass effect requiring decompressive surgery. She was managed conservatively with close monitoring. Serial neurological examinations were more valuable than repeated scans without clinical indication.
If a patient deteriorates despite anticoagulation, options may include transfer to a centre with neurocritical care, decompressive craniectomy for life-threatening mass effect, or endovascular therapy in selected cases. Evidence for endovascular treatment remains limited, so it is usually reserved for severe or worsening disease after specialist review.
Postpartum and breastfeeding considerations
The baby was well and breastfeeding had been initiated. The team discussed medication safety with the family. Heparins are generally considered compatible with breastfeeding because they have poor oral bioavailability and minimal transfer into milk. Warfarin is also commonly considered compatible with breastfeeding when longer oral anticoagulation is needed.
Direct oral anticoagulants are usually avoided during breastfeeding because safety data remain limited. Local guidance and specialist input are essential.
Before discharge, the patient was switched to an appropriate longer-term anticoagulation plan. Duration depends on whether the event was provoked, the extent of thrombosis, recurrence risk, and thrombophilia results. Many patients with a transient provoking factor receive several months of therapy, but the decision should be tailored.
What current literature and guidance suggest
Research and guideline statements consistently emphasise one point: postpartum CVST is a clinical diagnosis supported by imaging, not a diagnosis that can be excluded by a reassuring first impression.
The puerperium is prothrombotic. Pregnancy increases clotting factors, reduces fibrinolysis, and causes venous stasis. Delivery adds tissue injury, blood loss, dehydration risk, infection risk, and possible immobility. Caesarean section further increases venous thromboembolism risk compared with vaginal birth.
The clinical presentation is broad. Headache is the most common symptom in many reported series, but it is not specific. Seizures, focal weakness, aphasia, visual symptoms, papilloedema, altered sensorium, and features of raised intracranial pressure may occur. Some patients present like stroke. Others present like meningitis, migraine, eclampsia, or idiopathic intracranial hypertension.
Red flags in postpartum headache
Postpartum headache deserves urgent review when any of the following are present:
New severe headache or the worst headache reported by the patient
Progressive headache over hours to days
Headache that changes character after an initial diagnosis
Seizure, confusion, drowsiness, or syncope
Focal deficit such as weakness, aphasia, diplopia, or visual field loss
Papilloedema or persistent vomiting
Fever, meningism, or suspected sepsis
Hypertension, proteinuria, or features of preeclampsia
Recent caesarean delivery, dehydration, anaemia, infection, thrombophilia, or prior venous thromboembolism
D-dimer may be difficult to interpret in pregnancy and the puerperium. A normal result should not overrule strong clinical suspicion, especially when neurological signs are present.
A practical diagnostic pathway
A useful approach begins with a structured postpartum headache assessment.
Take a focused history. Ask about onset, peak intensity, postural nature, progression, visual symptoms, seizures, weakness, fever, neck pain, neuraxial anaesthesia, blood pressure history, bleeding, dehydration, infection, and thrombotic risk factors.
Examine fully. Check blood pressure repeatedly, not just once. Look for fever, neck stiffness, papilloedema, cranial nerve palsies, limb drift, speech disturbance, sensory loss, and cerebellar signs. A brief but careful neurological examination can prevent premature closure.
Order targeted tests. These may include complete blood count, platelets, renal and liver function, coagulation profile, urine protein assessment, and tests guided by sepsis or preeclampsia suspicion. Thrombophilia testing is usually not urgent in the acute phase and may be misleading during pregnancy, acute thrombosis, or anticoagulation.
Image early when red flags exist. MRI brain with MR venography is preferred when available. CT venography is a practical alternative and can be faster in many emergency settings. Non-contrast CT alone is not enough if suspicion remains.
Reassess after every new symptom. A patient treated for post-dural puncture headache who later develops seizure or focal deficit needs a fresh diagnosis, not only more analgesia.
How collaboration changes outcomes
Puerperal CVST sits between specialties. That is why multidisciplinary management is not optional. Each team sees a different part of the risk.
Obstetricians recognise postpartum physiology, surgical bleeding risk, preeclampsia overlap, wound status, and breastfeeding concerns. Neurologists guide seizure control, neuroimaging interpretation, anticoagulation decisions, and follow-up. Radiologists help choose the right imaging and identify subtle sinus or cortical vein thrombosis. Haematologists assess anticoagulant choice, duration, thrombophilia work-up, and recurrence risk. Critical care teams manage airway, consciousness, intracranial pressure concerns, and transfer decisions. Nurses often detect early neurological changes before anyone else.
The best systems use trigger points. For example, any postpartum patient with severe headache plus seizure, focal deficit, papilloedema, or altered sensorium should have urgent neuroimaging and specialist review. Clear escalation rules reduce dependence on chance.
Follow-up after discharge
Recovery does not end when headache improves. Follow-up should address:
Anticoagulation adherence and bleeding symptoms
Seizure recurrence and driving restrictions as per local law
Neurocognitive symptoms, mood, fatigue, and sleep disruption
Breastfeeding and medication compatibility
Repeat venous imaging when clinically indicated
Counselling about future pregnancy and thromboprophylaxis
Screening for thrombophilia when appropriate and timed correctly
In the presented case, the patient improved over 10 days. Speech normalised, headache settled, and no further seizures occurred. At follow-up, she had mild fatigue but no focal deficit. Future pregnancy counselling included early obstetric review, haematology input, hydration, mobilisation, and discussion of prophylactic anticoagulation based on her final risk assessment.
Key lessons from the case
The central lesson is simple: postpartum headache should be treated as a diagnosis in progress until dangerous causes are excluded.
CVST can mimic common puerperal conditions. A postural headache may initially suggest a dural puncture problem, and hypertension may point towards eclampsia. Yet progression, seizures, focal signs, papilloedema, or altered consciousness should reset the assessment.
Early venous imaging matters. CT or MRI without venography may miss the diagnosis. Anticoagulation remains the main treatment in most cases, even with haemorrhagic venous infarction, when guided by specialists. Severe cases need access to neurocritical care and, rarely, neurosurgical or endovascular options.
The strongest safeguard is collaboration. When obstetrics, neurology, radiology, haematology, critical care, nursing, and lactation services work together, patients receive faster diagnosis, safer anticoagulation, and better postpartum support. For medical practitioners and students, the practical takeaway is to listen carefully when a postpartum headache changes. That change may be the first clear sign of a treatable cerebral venous thrombosis.
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